The cellular basis of alcohol action in the nervous system is poorly understood. Recent studies have shown that alcohols can affect the function of certain neurotransmitter receptors; however, the cellular mechanisms involved in those effects have not been established. This project used electrophysiological techniques to study the cellular mechanisms of neurotransmitter receptor function and the interaction of alcohol with those mechanisms. The inhibition of NMDA receptor-mediated responses by ethanol was investigated in mouse hippocampal neurons using whole-cell patch-clamp recording. Ethanol decreased Emax of the agonist concentration-response curve, without affecting either the EC50 or the apparent Hill coefficient; a non-competitive mechanism. By contrast, ethanol inhibited the function of ATP-gated membrane ion channels (P2X receptors) by shifting the agonist concentration-response curve to the right in a parallel manner, increasing the EC50 without altering the maximal response (Emax). This effect could result either from competitive inhibition by ethanol or a decrease in the affinity of the receptor for ATP. The effect of ethanol on the activation and deactivation time-constants of ATP-activated current was studied, because competitive antagonists increase the activation time-constant without changing the deactivation time-constant, whereas a decrease in agonist affinity decreases the deactivation time-constant without affecting the activation time-constant. Ethanol decreased the deactivation time-constant without affecting the activation time-constant. The observations are consistent with an allosteric action of ethanol to decrease the agonist affinity of the receptor.